Replication stress, a source of epigenetic aberrations in cancer?

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Replication stress, a source of epigenetic aberrations in cancer? / Jasencakova, Zusana; Groth, Anja.

In: BioEssays, Vol. 32, No. 10, 10.2010, p. 847-55.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Jasencakova, Z & Groth, A 2010, 'Replication stress, a source of epigenetic aberrations in cancer?', BioEssays, vol. 32, no. 10, pp. 847-55. https://doi.org/10.1002/bies.201000055

APA

Jasencakova, Z., & Groth, A. (2010). Replication stress, a source of epigenetic aberrations in cancer? BioEssays, 32(10), 847-55. https://doi.org/10.1002/bies.201000055

Vancouver

Jasencakova Z, Groth A. Replication stress, a source of epigenetic aberrations in cancer? BioEssays. 2010 Oct;32(10):847-55. https://doi.org/10.1002/bies.201000055

Author

Jasencakova, Zusana ; Groth, Anja. / Replication stress, a source of epigenetic aberrations in cancer?. In: BioEssays. 2010 ; Vol. 32, No. 10. pp. 847-55.

Bibtex

@article{8a4192a0b42f11df825b000ea68e967b,
title = "Replication stress, a source of epigenetic aberrations in cancer?",
abstract = "Cancer cells accumulate widespread local and global chromatin changes and the source of this instability remains a key question. Here we hypothesize that chromatin alterations including unscheduled silencing can arise as a consequence of perturbed histone dynamics in response to replication stress. Chromatin organization is transiently disrupted during DNA replication and maintenance of epigenetic information thus relies on faithful restoration of chromatin on the new daughter strands. Acute replication stress challenges proper chromatin restoration by deregulating histone H3 lysine 9 mono-methylation on new histones and impairing parental histone recycling. This could facilitate stochastic epigenetic silencing by laying down repressive histone marks at sites of fork stalling. Deregulation of replication in response to oncogenes and other tumor-promoting insults is recognized as a significant source of genome instability in cancer. We propose that replication stress not only presents a threat to genome stability, but also jeopardizes chromatin integrity and increases epigenetic plasticity during tumorigenesis.",
author = "Zusana Jasencakova and Anja Groth",
year = "2010",
month = oct,
doi = "10.1002/bies.201000055",
language = "English",
volume = "32",
pages = "847--55",
journal = "BioEssays",
issn = "0265-9247",
publisher = "Wiley",
number = "10",

}

RIS

TY - JOUR

T1 - Replication stress, a source of epigenetic aberrations in cancer?

AU - Jasencakova, Zusana

AU - Groth, Anja

PY - 2010/10

Y1 - 2010/10

N2 - Cancer cells accumulate widespread local and global chromatin changes and the source of this instability remains a key question. Here we hypothesize that chromatin alterations including unscheduled silencing can arise as a consequence of perturbed histone dynamics in response to replication stress. Chromatin organization is transiently disrupted during DNA replication and maintenance of epigenetic information thus relies on faithful restoration of chromatin on the new daughter strands. Acute replication stress challenges proper chromatin restoration by deregulating histone H3 lysine 9 mono-methylation on new histones and impairing parental histone recycling. This could facilitate stochastic epigenetic silencing by laying down repressive histone marks at sites of fork stalling. Deregulation of replication in response to oncogenes and other tumor-promoting insults is recognized as a significant source of genome instability in cancer. We propose that replication stress not only presents a threat to genome stability, but also jeopardizes chromatin integrity and increases epigenetic plasticity during tumorigenesis.

AB - Cancer cells accumulate widespread local and global chromatin changes and the source of this instability remains a key question. Here we hypothesize that chromatin alterations including unscheduled silencing can arise as a consequence of perturbed histone dynamics in response to replication stress. Chromatin organization is transiently disrupted during DNA replication and maintenance of epigenetic information thus relies on faithful restoration of chromatin on the new daughter strands. Acute replication stress challenges proper chromatin restoration by deregulating histone H3 lysine 9 mono-methylation on new histones and impairing parental histone recycling. This could facilitate stochastic epigenetic silencing by laying down repressive histone marks at sites of fork stalling. Deregulation of replication in response to oncogenes and other tumor-promoting insults is recognized as a significant source of genome instability in cancer. We propose that replication stress not only presents a threat to genome stability, but also jeopardizes chromatin integrity and increases epigenetic plasticity during tumorigenesis.

U2 - 10.1002/bies.201000055

DO - 10.1002/bies.201000055

M3 - Review

C2 - 20726011

VL - 32

SP - 847

EP - 855

JO - BioEssays

JF - BioEssays

SN - 0265-9247

IS - 10

ER -

ID: 21661572